scholarly journals Photoprotective Potential of Penta-O-Galloyl-β-DGlucose by Targeting NF-κB and MAPK Signaling in UVB Radiation-Induced Human Dermal Fibroblasts and Mouse Skin

2015 ◽  
Vol 38 (11) ◽  
pp. 982-990 ◽  
Keyword(s):  
Mouse Skin ◽  
Mapk Signaling ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Uvb Radiation ◽  
Radiation Induced

Caffeic acid prevents UVB radiation induced photocarcinogenesis through regulation of PTEN signaling in human dermal fibroblasts and mouse skin

2018 ◽  
Vol 352 ◽  
pp. 87-96 ◽  
Author(s):  
Agilan Balupillai ◽  
Rajendra Prasad Nagarajan ◽  
Karthikeyan Ramasamy ◽  
Kanimozhi Govindasamy ◽  
Ganesan Muthusamy
Keyword(s):  
Caffeic Acid ◽  
Mouse Skin ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Uvb Radiation ◽  
Radiation Induced

scholarly journals Piper retrofractumVahl. Extract, as a PPARδand AMPK Activator, Suppresses UVB-Induced Photoaging through Mitochondrial Biogenesis and MMPs Inhibition in Human Dermal Fibroblasts and Hairless Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Jungon Yun ◽  
Changhee Kim ◽  
Mi-Bo Kim ◽  
Jae-Kwan Hwang
Keyword(s):  
Protein Kinase ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mouse Skin ◽  
Adenosine Monophosphate ◽  
Dermal Fibroblasts ◽  
Mitogen Activated Protein Kinase ◽  
Peroxisome Proliferator ◽  
Human Dermal Fibroblasts ◽  
Piper Retrofractum

Photoaging occurs by UVB-irradiation and involves production of reactive oxygen species (ROS) and overexpression of matrix metalloproteinases (MMPs), leading to extracellular matrix damage.Piper retrofractumVahl. is used as a traditional medicine for antiflatulence, expectorant, sedative, and anti-irritant; however, its antiphotoaging effect has not yet been studied. The current study investigated the antiphotoaging effect of standardizedPiper retrofractumextract (PRE) on UVB-damaged human dermal fibroblasts and hairless mouse skin. PRE treatment activated the peroxisome proliferator-activated receptor delta (PPARδ) and the adenosine monophosphate-activated protein kinase (AMPK), consequently upregulating mitochondrial synthesis and reducing ROS production. Additionally, PRE inhibited MMPs expression via suppressing mitogen-activated protein kinase (MAPK) and activator protein-1 (AP-1). PRE downregulated UVB-induced inflammatory reactions by inhibiting the nuclear factor-kappa B (NF-κB) activity. PRE also enhanced transforming growth factor-beta (TGF-β) and the Smad signaling pathway, thereby promoting procollagen gene transcription. Furthermore, oral administration of PRE (300 mg/kg/day) similarly regulated the signaling pathways and increased antioxidant enzyme expression, thus attenuating physiological deformations, such as wrinkle formation and erythema response. Collectively, these results suggest that PRE acts as a potent antiphotoaging agent via PPARδand AMPK activation.

scholarly journals Luteolin Prevents UVB-Induced Skin Photoaging Damage by Modulating SIRT3/ROS/MAPK Signaling: An in vitro and in vivo Studies

2021 ◽  
Vol 12 ◽  
Author(s):  
Jing Mu ◽  
Huisheng Ma ◽  
Hong Chen ◽  
Xiaoxia Zhang ◽  
Mengyi Ye
Keyword(s):  
Animal Experiments ◽  
Mapk Signaling ◽  
Dermal Fibroblasts ◽  
In Vivo Studies ◽  
Uvb Radiation ◽  
Skin Damage ◽  
Cellular Protection ◽  
Uvb Irradiation

The aim of this study was to investigate the role of luteolin in the mechanism of ultraviolet radiation B (UVB)-induced photoaging. An in vivo photoaging model was established using UVB irradiation of bare skin on the back of rats, and an in vitro photoaging model was established using UVB irradiation of human dermal fibroblasts (HDF). Skin damage was observed using hematoxylin-eosin (HE) and Masson staining, skin and cellular reactive oxygen species (ROS) levels were detected by DHE and DCF fluorescent probes, mitochondrial membrane potential was detected by JC-1 staining, and protein expressions were detected by immunofluorescence and Western Blot. Results from animal experiments showed that luteolin reduced UVB-induced erythema and wrinkle formation. Results from cellular assays showed that luteolin inhibited UVB-induced decrease in cell viability. In addition, in vitro and in vivo experiments showed that luteolin reduced oxidative stress levels, decreased activation of matrix metalloproteinases (MMPs) and increased collagen expression. Continued cellular experiments using 3-TYP, an inhibitor of Sirtuin 3 (SIRT3), revealed a loss of cellular protection by luteolin and a decrease in collagen, suggesting that luteolin acts by targeting and promoting SIRT3. luteolin is involved in the protection of skin cells against UVB radiation-induced ageing via the SIRT3/ROS/mitogen-activated protein kinases (MAPK) axis and it may be a promising therapeutic agent for the prevention of UVB photoaging.

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